Bisphenol A (BPA) is an endocrine disruptor widespread used in manufacturing of food, drink and sanitary plastic devices as well as thermal paper, resulting in a long-term exposure in humans. Relevant concentrations of BPA in human urine have been related to different pathologies. Indeed, it is well known that either direct exposure to BPA or maternal exposure during pregnancy, promotes metabolic alterations, reproductive disorders or cardiovascular diseases. Epigenetic mechanisms are thought to represent the most plausible targets through which BPA could have long-lasting effects since it can accumulate in adipose tissue of testicles allowing modifications in spermatozoa DNA methylation pattern, thus affecting indirectly the offspring. In this scenario, the aim of our work is to assess whether paternal exposure to BPA causes changes in DNA methylation which could lie behind phenotypic alterations in the progeny
